Diseases in plants cause considerable crop loss from year to year resulting both in economic deprivation to farmers and, in many parts of the world, to shortfalls in the nutritional provision for local populations. The widespread use of fungicides has provided considerable security against plant pathogen attack; however, despite $1 billion worth of expenditure on fungicides, worldwide crop losses amounted to approximately 10% of crop value in 1981 (James, 1981, Seed Sci. & Technol. 9: 679-685).
The severity of the destructive process of disease depends on the aggressiveness of the pathogen and the response of the host. One aim of most plant breeding programs is to increase the resistance of host plants to disease. Typically, different races of pathogens interact with different varieties of the same crop species differentially, and many sources of host resistance only protect against specific pathogen races. Furthermore, some pathogen races show early signs of disease symptoms, but cause little damage to the crop. Jones and Clifford (1983, Cereal Diseases, John Wiley) report that virulent forms of the pathogen are expected to emerge in the pathogen population in response to the introduction of resistance into host cultivars and that it is therefore necessary to monitor pathogen populations. In addition, there are several documented cases of the evolution of fungal strains that are resistant to particular fungicides. As early as 1981, Fletcher and Wolfe (1981, Proc. 1981 Brit. Crop Prot. Conf.) contended that 24% of the powdery mildew populations from spring barley and 53% from winter barley showed considerable variation in response to the fungicide triadimenol and that the distribution of these populations varied between varieties, with the most susceptible variety also giving the highest incidence of less susceptible types. Similar variation in the sensitivity of fungi to fungicides has been documented for wheat mildew (also to triadimenol), Botrytis (to benomyl), Pyrenophora (to organomercury), Pseudocercosporella (to MBC-type fungicides) and Mycosphaerella fijiensis to triazoles to mention just a few (Jones and Clifford, Cereal Diseases, John Wiley, 1983).
Maize Fusarium ear rots are caused by Fusarium verticillioides, F. proliferatum, and F. subglutinans. The importance of the disease is derived from the production of the mycotoxin fumonisin by the causal organisms (Compendium of Corn Diseases, 3rd ed., D. White Ed., APS Press, 1999). Contaminated grain can cause serious problems for the maize feed and food industries (Munkvold and Desjardins, 1997, Plant Disease 81(6):556-565). Fumonisins inhibit the biosynthesis of sphingolipids, changing the sphingolipid composition of a number of target tissues, and can cause a variety of diseases in animals that eat contaminated feeds (Munkvold and Desjardins, 1997). Consumption of maize contaminated with high levels of fumonisins has been epidemiologically associated with high levels of esophageal cancer in human populations in parts of the world where maize is a staple food (Munkvold and Desjardins, 1997). This situation is further complicated by the common occurrence of fumonisins in symptomless infected kernels (Desjardins and Plattner,1998, Plant Disease 82(8):953-958). Though Fusarium ear rots typically do not significantly affect yield, they do introduce mycotoxins to the grain, leading to the loss of grain and seed quality.
In view of the above, there is a real need for the development of technology that will allow the identification of specific races of pathogen fungi early in the infection process. By identifying the specific race of a pathogen before disease symptoms become evident in the crop stand, the agriculturist can assess the likely effects of further development of the pathogen in the crop variety in which it has been identified and can choose an appropriate fungicide if such application is deemed necessary.